Catalase Deficiency

Catalase deficiency means the body does not have enough of an enzyme called catalase. Catalase is a natural “safety” protein inside our cells. Its main job is to break down hydrogen peroxide (a strong oxidant our cells make during normal work) into water and oxygen very quickly. When catalase is very low or missing, hydrogen peroxide can build up. Extra hydrogen peroxide can damage mouth tissues and other cells. Most people with low catalase feel fine. A few people, especially with almost no catalase, can get painful mouth ulcers and tissue death after small injuries or infections. This rare condition is usually inherited from both parents and is often called acatalasia. Partial lack is sometimes called hypocatalasia or acatalasemia in older texts.

Catalase deficiency means the body does not make enough of an enzyme called catalase. Catalase normally breaks down hydrogen peroxide (a reactive, irritating chemical made inside our cells) into water and oxygen. When catalase is very low, hydrogen peroxide can build up. This extra peroxide can hurt nearby tissues by oxidative stress. The problem is usually caused by a change (mutation) in the CAT gene and is often inherited in an autosomal recessive way (you get one changed gene from each parent).

Most people with catalase deficiency feel well, but some get painful mouth ulcers, gum infections, bad breath, and delayed wound healing in the mouth (historically called acatalasia or Takayama disease). Because peroxide is not cleared well, peroxide-containing mouthwashes can burn the mouth. Scientists also study possible links to diabetes, periodontal disease, and other oxidative-stress problems, but these links can be different from person to person. Diagnosis is based on very low catalase activity in blood and, sometimes, CAT gene testing. Treatment focuses on gentle mouth care, infection control, avoiding sources of hydrogen peroxide, and reducing oxidative stress safely.

What catalase does

Hydrogen peroxide forms in many normal body reactions. It is useful in small amounts but harmful in large amounts. Catalase sits mainly in peroxisomes (small clean-up rooms inside cells). It quickly turns hydrogen peroxide into water and oxygen. This action protects the mouth lining, gums, skin, red blood cells, and many other tissues from oxidative injury. If catalase is too low, cells rely more on other antioxidants such as glutathione peroxidase (GPx) and superoxide dismutase (SOD). That back-up often works, which is why many people with catalase deficiency have no symptoms. Problems show up most clearly where bacteria and small injuries often make extra hydrogen peroxide—the mouth.

Other names

• Acatalasia (very low or no catalase activity)

• Acatalasemia / acatalasæmia (older spellings)

• Hypocatalasia (partially low catalase)

• Takahara disease (historic name, linked to mouth gangrene in severe cases)

• Catalase (CAT) gene deficiency

These terms often refer to the same basic problem: unusually low catalase activity, from almost none (acatalasia) to moderately low (hypocatalasia).

Types

1. Genetic acatalasia (complete or near-complete): Catalase activity is almost absent. This is the classic inherited form. Symptoms can include severe mouth ulcers after small injuries or infections.

2. Genetic hypocatalasia (partial): Catalase level is reduced but not zero. Most people have no symptoms or only mild problems such as recurring gum inflammation.

3. Carrier state (heterozygous): One normal and one altered CAT gene. Catalase is lower than average but often still sufficient; usually no symptoms.

4. Functional or secondary low catalase: Catalase exists but works less well because of other health conditions (for example, severe iron lack, long-term uncontrolled diabetes, or general oxidative stress). This is not the classic inherited acatalasia but can look similar on a simple activity test.

5. Tissue-skewed low catalase: Catalase is much lower in some tissues (often red blood cells or the mouth lining) than in others.

6. Transient low catalase: Short-term drop during an acute illness or major stress, with return toward normal after recovery.

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Causes

The first group are primary genetic causes (changes in the CAT gene). The rest are associated or contributing factors that can lower measured catalase activity or increase peroxide stress. Your doctor will sort out which apply to you.

1. Loss-of-function CAT gene mutation (autosomal recessive): Both copies of the CAT gene do not work well, so the enzyme is missing or too weak.

2. Missense mutation: A single “letter” change in the CAT gene makes catalase fold incorrectly and work poorly.

3. Nonsense or frameshift mutation: A change that cuts the enzyme short so it cannot function.

4. Splice-site mutation: A change that disrupts how the gene is processed, producing a faulty enzyme.

5. Promoter or regulatory variant: The gene is intact, but its “on/off” switch is weak, so less enzyme is made.

6. Compound heterozygosity: Two different harmful variants (one from each parent) combine to cause very low activity.

7. Founder mutations in certain families/regions: A historical variant that became more common in a local group can lead to clustered cases.

8. Consanguinity (parents related by blood): Increases the chance that a child receives the same rare harmful variant from both parents.

9. Peroxisomal biogenesis disorders (rare): Catalase cannot reach its normal cell “room” (peroxisome), so activity is functionally low in that compartment.

10. Severe iron deficiency: Catalase uses heme (which needs iron). Low iron can reduce fully active catalase.

11. Severe protein malnutrition: Less raw material to build enzymes can reduce catalase production.

12. Chronic uncontrolled diabetes: Oxidative stress and glycation can depress catalase activity and overwhelm backup systems.

13. Chronic inflammatory states (periodontitis, recurrent infections): Constant oxidant load can inactivate catalase faster than the body can replace it.

14. Heavy metal exposure (e.g., lead) or certain toxicants: Can damage enzymes directly and impair antioxidant systems.

15. Liver failure or advanced liver disease: The liver makes and renews many enzymes; severe disease can lower catalase in blood cells and tissues.

16. Thyroid dysfunction (especially severe hypothyroidism): Can slow overall enzyme turnover and alter oxidative balance.

17. Aging: Catalase levels and activity can decline with age in some tissues.

18. Certain medications or chemicals that raise peroxide load: For example, frequent strong peroxide mouthwashes can injure oral tissue if catalase is very low.

19. Smoking: Adds oxidants and reduces antioxidant capacity over time.

20. Acute severe infection or sepsis: Massive oxidant stress can temporarily reduce functional catalase activity.

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Symptoms and signs

Many people have no symptoms. Problems, when they happen, are often in the mouth.

1. Painful mouth ulcers that start after minor injury, dental work, or infection.

2. Tissue breakdown in the mouth (ulcer with gray or black base), sometimes called “gangrene” in old reports.

3. Gum swelling and bleeding (gingivitis), especially with poor oral hygiene.

4. Bad breath from infected or dead tissue.

5. Slow healing after tooth extraction or small cuts in the mouth.

6. Recurring mouth infections (bacterial or fungal).

7. Tooth pain or loose teeth if gum disease advances.

8. Burning or stinging with peroxide rinses more than expected.

9. Dry or sore mouth during flares.

10. Skin sores that heal slowly after minor trauma (less common).

11. Fatigue during active infection or chronic inflammation.

12. Low-grade fever when ulcers are infected.

13. Swollen lymph nodes under the jaw during mouth infections.

14. Weight loss if eating is painful for many days.

15. Anxiety about eating and speaking due to mouth pain.

Important: severe mouth tissue death is uncommon and usually linked to the complete genetic form (acatalasia). Many people with low catalase never get these problems.

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Diagnostic tests

A) Physical exam

1. Detailed history and family history: Your clinician asks about mouth ulcers, dental work, infections, healing time, peroxide sensitivity, and relatives with similar issues. This helps spot an inherited pattern and triggers focused testing.

2. Full oral cavity exam: Careful look at gums, tongue, cheeks, palate, and extraction sites for ulcers, dead tissue, swelling, pus, or fungal plaques. The pattern guides next steps.

3. Periodontal assessment by a dentist: Probing gum pockets, checking tooth mobility, and plaque load. It quantifies gum disease that may flare in low-catalase states.

4. Skin and wound check: Looks for slow-healing sores elsewhere and signs of secondary infection, which support the overall picture.

B) Manual (bedside) tests

These are screening demonstrations only. They do not replace proper lab tests and should be done by trained staff with safety in mind.

5. Bedside blood-drop peroxide “bubble” test: A drop of your blood is touched with a drop of dilute hydrogen peroxide. Normal catalase makes brisk bubbles (oxygen). Very few bubbles suggest low catalase. This is quick but only qualitative.

6. Filter-paper catalase spot test (semi-quantitative): A standardized spot card and peroxide give a timed bubble/fizz score. It is still rough, but a bit more consistent than the simple drop test.

7. Oral swab peroxide test (research/clinical screening): A clinician places a tiny amount of dilute peroxide on an oral swab from the cheek or gum and observes bubble formation. Reduced bubbling can support the suspicion when matched with symptoms. Professional precautions are required to avoid irritation.

C) Laboratory & pathological tests

8. Red blood cell (RBC) catalase activity assay (spectrophotometry): The gold-standard functional test. It measures how fast your RBCs break down hydrogen peroxide. Very low rate confirms catalase deficiency.

9. Leukocyte or fibroblast catalase activity: If RBC results need confirmation, catalase can be measured in white cells or skin fibroblasts to rule out RBC-specific artifacts.

10. CAT gene sequencing: Reads the CAT gene letters to find harmful variants. Confirms inherited acatalasia or hypocatalasia and helps with family counseling.

11. CAT gene deletion/duplication analysis: Looks for missing or extra gene segments if standard sequencing is normal but activity is very low.

12. Peroxisomal enzyme panel: Measures other peroxisome enzymes to check for rare peroxisomal disorders that could secondarily affect catalase location or function.

13. Iron and heme status (CBC, ferritin, transferrin, iron): Low iron can impair heme-containing enzymes like catalase; this helps identify a fixable contributor.

14. Oxidative stress biomarkers (e.g., malondialdehyde, 8-OHdG) and antioxidant panel (SOD, GPx): Show the balance between oxidants and antioxidants and help tailor supportive care.

15. Glucose and HbA1c: Screens for diabetes, which can worsen oxidative stress and mouth disease; managing diabetes can reduce flares.

16. Biopsy/culture of an active oral ulcer (when needed): Rules out cancer, deep fungal infection, noma-like infections, or other causes of tissue death; guides targeted antibiotics or antifungals.

D) Electrodiagnostic tests

There is no electrodiagnostic test that directly “measures” catalase. These tests are adjuncts when symptoms point to complications.

17. Electrocardiogram (ECG): Used during severe infection, dehydration, or pain to monitor heart stress and electrolytes; helpful in urgent care, not for diagnosis of catalase deficiency itself.

18. Nerve conduction studies/EMG (select cases): If a person with low catalase also has diabetes and nerve symptoms (numbness, burning), this evaluates neuropathy that may complicate mouth care and wound healing.

E) Imaging tests

19. Dental panoramic X-ray (orthopantomogram): Shows bone loss, hidden dental abscesses, or osteomyelitis around a chronic ulcer or extraction site.

20. CT or MRI of jaw/neck (for severe or spreading infection): Maps the extent of soft-tissue involvement and guides surgery or drainage if needed.

Non-pharmacological treatments

(15 Physiotherapy/physical & oral care, 5 Mind–body, 2 Gene-therapy/biologic concepts, 3 Educational therapy)

A) Physiotherapy / physical & oral-care strategies

1. Peroxide-free oral hygiene routine
   Purpose: Prevent ulcers and gum disease without irritating agents.
   Mechanism/benefit: Use a soft toothbrush, non-foaming fluoride toothpaste, and alcohol-free, peroxide-free rinses; this lowers mechanical and chemical injury, which reduces oxidative stress and secondary infection.

2. Warm saline or baking-soda rinses
   Purpose: Soothe pain, keep pH neutral, and wash debris.
   Mechanism: ½ tsp salt or ½ tsp baking soda in a cup of warm water, swish gently; buffers acids, reduces irritants, and supports healing.

3. Oral moisture support
   Purpose: Protect dry mouth (xerostomia) that can worsen ulcers.
   Mechanism: Frequent sips of water, sugar-free xylitol lozenges, humidifier at night; saliva protection reduces friction and bacterial overgrowth.

4. Low-level laser therapy (LLLT/photobiomodulation) for oral ulcers
   Purpose: Speed healing and reduce pain without drugs.
   Mechanism: Safe light doses modulate mitochondrial signaling and local inflammation, encouraging tissue repair.

5. Cold therapy (ice chips)
   Purpose: Short-term pain relief in active ulcers.
   Mechanism: Mild vasoconstriction numbs area and decreases inflammatory mediators.

6. Gentle jaw range-of-motion exercises
   Purpose: Prevent stiffness when chewing is painful.
   Mechanism: Slow opening/closing and side glides maintain TMJ mobility and reduce compensatory muscle spasm.

7. Orofacial myofunctional therapy
   Purpose: Improve lip/tongue posture and reduce trauma from biting or friction.
   Mechanism: Targeted exercises change muscle habits, lowering repeated mechanical injury to mucosa.

8. Tongue and cheek protective barriers
   Purpose: Prevent rubbing on sharp teeth/edges.
   Mechanism: Use dental wax or silicone guards advised by a dentist to reduce friction and new ulcer formation.

9. Professional periodontal care (non-surgical)
   Purpose: Control plaque and calculus to prevent infections.
   Mechanism: Regular scaling and root planing reduce bacterial load and inflammatory triggers for ulceration.

10. Nutritional counseling for soft, non-irritating diets
    Purpose: Maintain nutrition during flares.
    Mechanism: Switch to soft, lukewarm, bland foods to avoid mechanical and thermal injury; supports healing.

11. Topical barrier pastes (non-medicated base)
    Purpose: Shield ulcers from food and saliva.
    Mechanism: Protective pastes (e.g., carboxymethylcellulose base) create a physical film that reduces pain with eating.

12. TMJ/posture physiotherapy
    Purpose: Ease secondary jaw and neck pain from guarded chewing.
    Mechanism: Neck/scapular stabilization and jaw relaxation techniques balance muscles and reduce referred pain.

13. Good sleep routine
    Purpose: Enhance tissue repair and immune balance.
    Mechanism: Consistent sleep times and cool, dark room improve growth-and-repair phases that help mucosal healing.

14. Smoking cessation & alcohol avoidance
    Purpose: Cut oxidative and chemical injury in the mouth.
    Mechanism: Removing major irritants lowers inflammation and speeds healing.

15. Early dental visit for sharp restorations
    Purpose: Remove local trauma sources.
    Mechanism: Smoothing or adjusting restorations and edges prevents repeated mucosal injuries.

B) Mind–body approaches

16. Mindfulness-based stress reduction (MBSR)
    Purpose: Reduce flare triggers linked with stress.
    Mechanism/benefit: Calms HPA axis and sympathetic tone; people often report less pain perception and fewer stress-related flares.

17. Cognitive behavioral therapy (CBT) for chronic pain
    Purpose: Improve coping with recurrent ulcers and meal anxiety.
    Mechanism: Reframes pain thoughts and builds graded exposure to normal eating habits.

18. Diaphragmatic breathing
    Purpose: Short-term pain and anxiety control before meals or dental care.
    Mechanism: Increases vagal tone, lowers heart rate, reduces muscle tension around jaw/neck.

19. Guided imagery/relaxation before oral care
    Purpose: Improve adherence to gentle but regular hygiene.
    Mechanism: Lowers anticipatory pain response so brushing/rinsing are consistent.

20. Sleep hygiene coaching
    Purpose: Keep circadian rhythm stable for healing.
    Mechanism: Regular schedule, light control, and device limits improve sleep quality and immunity.

C) Gene-therapy / biologic concepts (investigational — not standard care)

21. AAV-based CAT gene delivery
    Purpose: Restore catalase production in tissues.
    Mechanism/benefit: A harmless viral vector carries a healthy CAT gene to cells so they can make catalase; studied in labs/early models.

22. mRNA-lipid nanoparticle (LNP) catalase therapy
    Purpose: Temporary boost of catalase enzyme.
    Mechanism: LNPs deliver CAT mRNA so cells make catalase for a limited time; still experimental.

D) Educational therapies

23. Condition-specific education
    Purpose: Empower safe daily choices.
    Mechanism: Teach what catalase does, why peroxide is harmful here, and how to pick peroxide-free products.

24. Self-management action plan
    Purpose: Standard steps for flares.
    Mechanism: Simple plan: soothe → protect → disinfect gently (no peroxide) → call dentist/doctor if red flags.

25. Family genetic counseling
    Purpose: Understand inheritance and testing.
    Mechanism: Explains autosomal recessive patterns, carrier testing, and options for family planning.

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Drug treatments

(Evidence-informed options used to manage ulcers, pain, and infections. Always individualize with your clinician. Doses are typical adult references; adjust for age, weight, kidney/liver function, pregnancy, and interactions.)

1. Chlorhexidine 0.12% mouth rinse (antiseptic)
   Dose/time: 15 mL swish 30 seconds, spit, twice daily for 7–14 days (avoid immediately before/after toothbrushing).
   Purpose: Reduce oral bacteria during ulcer flares.
   Mechanism: Disrupts microbial membranes.
   Side effects: Temporary taste change, staining, rare irritation.

2. Topical lidocaine 2% viscous (local anesthetic)
   Dose/time: 5–10 mL swish and spit every 3–4 hours as needed; use carefully to avoid numb-bite injuries.
   Purpose: Pain control for eating/oral care.
   Mechanism: Blocks sodium channels.
   Side effects: Numbness, rare systemic toxicity if swallowed in excess.

3. Triamcinolone acetonide 0.1% dental paste (topical corticosteroid)
   Dose/time: Thin film on ulcer 2–4 times daily for up to 7–10 days.
   Purpose: Decrease inflammation and pain.
   Mechanism: Down-regulates cytokines.
   Side effects: Local Candida overgrowth if prolonged; thin mucosa with overuse.

4. Dexamethasone elixir (topical rinse) (corticosteroid)
   Dose/time: 0.5 mg/5 mL, swish and spit qid for 5–7 days in severe flares under supervision.
   Purpose: Short burst anti-inflammation.
   Side effects: Thrush risk; systemic absorption if swallowed.

5. Amoxicillin–clavulanate (antibiotic)
   Dose/time: 875/125 mg twice daily for 5–7 days for spreading odontogenic infection or abscess per dental exam.
   Purpose: Treat bacterial infection.
   Mechanism: β-lactam with β-lactamase inhibitor.
   Side effects: GI upset, allergy, diarrhea.

6. Metronidazole (antibiotic, anaerobes)
   Dose/time: 500 mg three times daily for 3–5 days for necrotizing gingivitis/anaerobic burden; often added to amoxicillin in severe periodontal infection.
   Side effects: Metallic taste, avoid alcohol, neuropathy with long use.

7. Clindamycin (antibiotic for penicillin allergy)
   Dose/time: 300 mg four times daily 5–7 days when indicated.
   Side effects: Diarrhea, C. difficile risk.

8. Acetaminophen (paracetamol) (analgesic)
   Dose/time: 500–1,000 mg every 6–8 hours (max 3,000–4,000 mg/day depending on local guidance).
   Purpose: Pain/fever relief.
   Mechanism: Central analgesia.
   Side effects: Liver toxicity if overdosed or with alcohol.

9. Ibuprofen (NSAID; avoid if GI, kidney, or bleeding risk)
   Dose/time: 200–400 mg every 6–8 hours with food during short flares.
   Purpose: Pain and inflammation.
   Mechanism: COX inhibition → ↓prostaglandins.
   Side effects: Stomach upset, bleeding risk, kidney strain.

10. Benzocaine oral gel (topical anesthetic; use sparingly)
    Dose/time: Thin film up to qid.
    Purpose: Spot pain relief.
    Mechanism: Local sodium channel block.
    Side effects: Methemoglobinemia risk (rare), local allergy.

11. Nystatin oral suspension (antifungal)
    Dose/time: 4–5 mL qid, swish and swallow/spit for 7–14 days if steroid-related thrush develops.
    Side effects: Nausea (uncommon).

12. Fluconazole (systemic antifungal if needed)
    Dose/time: 100–200 mg daily 7–14 days per clinician if candidiasis is significant.
    Side effects: Liver enzyme rise, interactions (CYP).

13. Topical sucralfate suspension (off-label in mouth)
    Dose/time: 1 g/10 mL, swish and spit qid.
    Purpose: Protective coating of ulcers.
    Mechanism: Adheres to ulcer base forming a barrier.
    Side effects: Constipation (if swallowed).

14. Folic acid or B12 when deficient
    Dose/time: Folate 1 mg daily; B12 per deficiency route (oral 1,000 mcg daily or IM schedule).
    Purpose: Support mucosal turnover where labs confirm deficiency.
    Mechanism: DNA synthesis for epithelial repair.
    Side effects: Generally well-tolerated.

15. Topical hyaluronic acid gel
    Dose/time: Apply 2–3 times daily.
    Purpose: Moist wound healing and pain reduction.
    Mechanism: Hydrates matrix and supports epithelial migration.
    Side effects: Rare local irritation.

Important: There is no standard “catalase replacement medicine” approved for routine clinical use in this condition. Management focuses on gentle care, infection control, pain relief, and reducing oxidative triggers.

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Dietary molecular supplements

(Discuss with your clinician; avoid interactions and excessive doses.)

1. Vitamin C (ascorbic acid) — 500 mg twice daily
   Function/mechanism: Water-soluble antioxidant; supports collagen and wound healing; scavenges peroxide-related radicals.

2. Vitamin E (mixed tocopherols/tocotrienols) — 200–400 IU daily
   Mechanism: Lipid-phase antioxidant protecting cell membranes from oxidative damage.

3. N-Acetylcysteine (NAC) — 600 mg once or twice daily
   Mechanism: Cysteine donor → boosts intracellular glutathione; helps neutralize peroxides.

4. Alpha-lipoic acid — 300 mg twice daily
   Mechanism: Redox cofactor that regenerates vitamins C and E; supports nerve and endothelial health.

5. Coenzyme Q10 (ubiquinone) — 100–200 mg daily
   Mechanism: Mitochondrial electron transport and antioxidant roles; may aid periodontal support.

6. Selenium — 100 mcg daily (do not exceed 200 mcg/day without advice)
   Mechanism: Cofactor for glutathione peroxidases that detoxify peroxides.

7. Zinc — 10–20 mg elemental daily (short courses)
   Mechanism: Epithelial repair and immune function; excessive long-term zinc can lower copper.

8. Curcumin (with piperine) — 500 mg twice daily
   Mechanism: NF-κB modulation and antioxidant effects; may reduce oral inflammation (watch drug interactions).

9. Green tea extract (EGCG) — 200–300 mg daily
   Mechanism: Polyphenol antioxidants; may support periodontal health (avoid late evening if sensitive to caffeine).

10. Resveratrol — 100–250 mg daily
    Mechanism: Antioxidant signaling (SIRT pathways) and endothelial support; clinical impact varies by person.

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Regenerative / stem-cell” drugs

Safety note: There are no approved stem-cell or “immune-booster” drugs specifically for catalase deficiency. Items below are experimental or context-specific; dosing for this condition is not established and should not be attempted outside clinical trials or specialist care.

1. PEG-catalase (pegylated catalase) — investigational
   Function/mechanism: Long-circulating catalase enzyme to break down hydrogen peroxide.

2. Catalase-loaded nanoparticles or liposomes — investigational
   Mechanism: Targeted delivery of active catalase to tissues with oxidative stress.

3. AAV-mediated CAT gene therapy — investigational
   Mechanism: Delivers a working CAT gene to cells for endogenous catalase production.

4. mRNA-LNP catalase — investigational
   Mechanism: Temporary cellular production of catalase after mRNA uptake.

5. SOD/catalase mimetics (e.g., EUK-134, Mn porphyrins) — investigational
   Mechanism: Small molecules that mimic antioxidant enzymes to neutralize ROS including peroxides.

6. Keratinocyte growth factor (palifermin) — context-specific
   Mechanism: Enhances mucosal repair; approved for chemo-related mucositis, not for catalase deficiency, but illustrates a regenerative pathway under specialist care.

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Surgeries / procedures

1. Surgical debridement of necrotic oral tissue
   Why done: Remove dead/infected tissue in severe gangrenous stomatitis to allow healing and stop spread.

2. Incision and drainage of oral/facial abscess
   Why done: Evacuate pus, reduce pressure, and clear infection source when antibiotics alone are not enough.

3. Periodontal flap surgery
   Why done: Access deep pockets for thorough decontamination when advanced periodontitis threatens teeth.

4. Soft-tissue grafts (e.g., free gingival graft)
   Why done: Cover recurrently traumatized areas, increase keratinized tissue, and reduce ulcer recurrence from friction.

5. Tooth extraction of non-restorable sources of infection
   Why done: Remove persistent infection/trauma sources to protect overall oral health.

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Preventions

1. Use peroxide-free dental products and avoid hydrogen-peroxide mouthwash.

2. Brush gently with a soft brush; replace brush every 3 months.

3. Floss or use interdental cleaners without snapping into gums.

4. Rinse with warm saline or baking-soda water after meals.

5. Keep lips/tongue moist; sip water often.

6. Stop smoking and avoid alcohol-based rinses.

7. Choose soft, lukewarm, non-spicy foods during flares.

8. See a dentist regularly for cleaning and to smooth sharp edges.

9. Manage stress and sleep well to support healing.

10. Control other conditions that worsen oral health (e.g., diabetes).

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When to see a doctor or dentist

• Ulcers or mouth pain lasting >2 weeks or getting worse.

• Fever, facial swelling, or spreading redness.

• Trouble swallowing, drooling, or trismus (can’t open mouth).

• Bad breath with pus from gums or a loose tooth.

• Ulcers keep coming back despite careful peroxide-free care.

• Signs of thrush (white plaques) especially after steroid use.

• You are pregnant, immunocompromised, or have diabetes and mouth problems.

• You need help choosing safe dental products (to avoid peroxide).

• You want genetic counseling or family testing.

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Foods to eat and to avoid

Eat more of these (especially during flares):

1. Soft porridge, oatmeal, or congee (lukewarm).

2. Mashed potatoes, steamed rice, soft noodles.

3. Scrambled eggs, soft tofu, yogurt.

4. Soft, ripe fruits (banana, ripe mango) and stewed apples/pears.

5. Well-cooked vegetables (carrots, pumpkin, squash).

6. Smooth soups and broths (not hot or spicy).

7. Fish or chicken shredded into soft pieces.

8. Healthy fats (olive oil, avocado) to maintain calories.

9. Plain cottage cheese or paneer (if tolerated).

10. Plenty of water and herbal teas (not hot).

Avoid or limit:

1. Hydrogen-peroxide mouth rinses (not a food, but crucial).

2. Very hot foods and drinks.

3. Spicy or acidic foods (chili, citrus, pineapple) during flares.

4. Hard, sharp foods (chips, crusts, nuts) that cut mucosa.

5. Alcohol (including alcohol-based mouth rinses).

6. Highly sugary snacks/drinks that feed plaque bacteria.

7. Very salty or vinegary foods that sting ulcers.

8. Smoking or smokeless tobacco.

9. Strong mint/menthol products that irritate.

10. Ultra-processed foods that add inflammatory load.

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Frequently Asked Questions (FAQs)

1) What exactly is catalase?
Catalase is an enzyme in many cells. It quickly splits hydrogen peroxide into water and oxygen, protecting tissues from oxidative harm.

2) What causes catalase deficiency?
Most cases come from changes in the CAT gene. It is often inherited in an autosomal recessive way.

3) Are all people with catalase deficiency sick?
No. Many have no symptoms. Others develop mouth ulcers, gum disease, and delayed healing, especially if exposed to irritants like peroxide.

4) Why does the mouth get ulcers first?
The mouth constantly faces friction, microbes, and minor injuries. Without good peroxide clearance, oxidative stress can trigger ulcers and infections.

5) Is hydrogen-peroxide mouthwash safe for me?
Usually no. In catalase deficiency, peroxide can irritate and worsen ulcers. Choose peroxide-free, alcohol-free rinses.

6) How is it diagnosed?
Blood tests show very low catalase activity. Genetic testing of CAT can confirm the cause.

7) Can it be cured?
There is no standard cure yet. Supportive care works well for many. Gene-therapy and enzyme-delivery ideas are under research.

8) What is the long-term outlook?
With gentle mouth care, infection control, and healthy habits, most people do well. Regular dental care greatly lowers complications.

9) Is it contagious?
No. It is a genetic condition.

10) Do I need special dental care?
Yes—avoid peroxide products, treat infections early, and schedule regular cleanings. Ask dentists to smooth sharp edges and use gentle techniques.

11) Will antioxidants help?
Some people benefit from a balanced antioxidant plan (diet + carefully chosen supplements). Discuss doses and interactions with your clinician.

12) Can children be tested?
Yes. Pediatricians/dentists can coordinate enzyme testing and genetic counseling depending on symptoms and family plans.

13) What about pregnancy?
Use the safest, simplest mouth care. Many drugs and supplements change in pregnancy—always check with your obstetrician and dentist.

14) Are there other body problems linked to low catalase?
Research explores links with diabetes risk and oxidative-stress disorders, but effects vary. Your clinician can personalize screening.

15) What is the single most important daily habit?
A peroxide-free, gentle oral routine plus early attention to any ulcer or infection.

Disclaimer: Each person’s journey is unique, treatment plan, life style, food habit, hormonal condition, immune system, chronic disease condition, geological location, weather and previous medical  history is also unique. So always seek the best advice from a qualified medical professional or health care provider before trying any treatments to ensure to find out the best plan for you. This guide is for general information and educational purposes only. Regular check-ups and awareness can help to manage and prevent complications associated with these diseases conditions. If you or someone are suffering from this disease condition bookmark this website or share with someone who might find it useful! Boost your knowledge and stay ahead in your health journey. We always try to ensure that the content is regularly updated to reflect the latest medical research and treatment options. Thank you for giving your valuable time to read the article.

The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members

Last Updated: September 01, 2025.

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